1. Etiology of stress-induced hupocalcemia : Muscarinic antagonist, gastric vagotomy, gastrin release inhibitors or histamine H_2 receptor antagonists diminished the immobilization (IMB) -induced hypocalcemia. The concentration of serum gastrin increased significantly during IMB.Either an antrectomy (removal of the source of gastrin) or a fundectomy (depriving the origin of gastric histamine and gastric acid) was also sufficient for eliminating IMB-induced hypocalcemia. These findings suggest that the antrum and the fundus of the stomach play essential roles in IMB-induced hypocalcemia through the vagus-induced release of gastrin and histamine.2. Hypothalamic involvement in stress-induced hypocalcemia : Bilateral lesions of the ventromedial nucleus of the hypothalamus (VMH), but not those of the paraventricular hypothalamic nucleus or the lateral hypothalamic area, eliminated immobilization (IMB)-induced hypocalcemia, and electrical stimulation of the VMH decrease the blood calcium level.3. Hypothalamic linkage of stress-induced hypocalcemia and gastric lesions are closely related and are also influenced by behavioral responsiveness in a strain dependent manner. VMH lesion diminished or attenuated stress-induced hypocalcemia, gastric lesions, and behavioral despair, while the PVN has an opposite effect.4. Hypothalamic control of blood calcium homeostasis : Stimulation studies revealed that the LHA and the PVN have a hypocalcemic function which is mediated, at least n part, bby the vagus nerve innervating the stomach and the thyroid/parathyhroid glands, respectively.5. Central effect of parathyroid hormone : Intracerebroventricular injection of PTH prevented urethan-induced hypocalcemia. Hypothalamic injection of PTH prevented urethan-induced hypocalcemia. Hypothalamic injection of PTH also showed a hypercalcemic effect. PTH inhibited activity of VMH neurons through postsynaptic mechanism mediated by PTH receptors.